MiR-183 regulates milk fat metabolism via MST1 in goat mammary epithelial cells
The nutritional value of goat milk largely depends on its fatty acid content and composition. MicroRNAs (miRNAs) are a class of RNA molecules 18–25nt in length that regulate gene expression and play crucial roles in several biological processes, including fatty acid metabolism. In this study, we ana...
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Published in: | Gene Vol. 646; pp. 12 - 19 |
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Main Authors: | , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Netherlands
Elsevier B.V
10-03-2018
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Subjects: | |
Online Access: | Get full text |
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Summary: | The nutritional value of goat milk largely depends on its fatty acid content and composition. MicroRNAs (miRNAs) are a class of RNA molecules 18–25nt in length that regulate gene expression and play crucial roles in several biological processes, including fatty acid metabolism. In this study, we analyzed the correlation between differentially expressed miRNAs in goat mammary tissue and the fatty acid composition of goat milk by using Pearson correlations. Results revealed that levels of miR-183 were highly and positively correlated with the fatty acid content in the milk. In addition, we demonstrated that overexpression of miR-183 inhibits milk fat metabolism and inhibition of miR-183 promotes milk fat metabolism. Using Western blot, we demonstrate that MST1, one of the major elements of the Hippo signaling pathway, is a target of miR-183. Immunofluorescence assays revealed that miR-183 targets MST1 in the cytoplasm. In summary, data indicate that miR-183 inhibits the metabolism of milk fat by targeting the MST1 gene in the cytoplasm in goat mammary epithelial cells.
•The relationship between miRNA and fatty acids.•miR-183 played an important role in fat metabolism.•miR-183 inhibits the metabolism of milk fat by targeting the MST1 gene in the cytoplasm in goat mammary epithelial cells. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0378-1119 1879-0038 |
DOI: | 10.1016/j.gene.2017.12.052 |